The chlorinated dibenzo-p-dioxins and dibenzofurans are trace contaminants formed during the commercial synthesis of a number of chlorinated phenolic products: 2,4,5-T, a herbicide; pentachlorophenol, a bacteriostat; and the polychlorobiphenyls, heat exchange fluid and plasticizers. 2,3,7,8-Tetrachlorodibenzo-p-dioxin, the prototype compound, is one of the most potent small molecule toxins and teratogens known, and because of its toxicity, chemical stability, prolonged survival in the biosphere, and inadvertent dispersion in our environment, it poses a potential health hazard. One of the most sensitive and earliest biochemical responses evoked by TCDD is the induction of aryl hydrocarbon hydroxylase activity (AHH). The toxic potency of the chlorinated dibenzo-p-dioxins corresponds with their potency to induce AHH activity. The stereospecific recognition of the dioxins resides in the recognition site, the induction receptor site, which initiates the genetic expression of hydroxylase activity. We propose to characterize this receptor and study its mechanism of action and in turn its relationship to dioxin toxicity. We also propose to study the teratogenic action and chloracne formation evoked by these compounds.